A Physis Set Up to Fail

Commentary The topography of the proximal femoral physis is a determinant of its stability. In an anatomic study of the contours of the physis of the proximal femur in dry skeletal specimens, Liu et al. described a tubercle projecting from the epiphysis at its posterolateral aspect, in a shape somewhat like that of a keystone and interlocking with a corresponding fossa at the metaphyseal aspect1. The location of the epiphyseal tubercle coincides with the site of maximum stress on the physis2. During growth, the perimeter of the epiphysis develops a “lip,” so by early adolescence, it resembles an inverted cup. Typically, the height of the “lip of the cup” increases during later adolescence, while the tubercle becomes relatively smaller1. The present study by Novais et al. offers a substantial contribution to our knowledge of the pathogenesis of slipped capital femoral epiphysis (SCFE). Their previous work has shown that the epiphyseal tubercle is smaller in hips with SCFE, while the metaphyseal fossa is larger3. The present study shows that abnormalities of the osseous contours of the epiphysis exist in children with obesity. Using sophisticated 3D imaging of the proximal femur, derived from hip or pelvic computed tomography (CT) scans (most as part of the diagnostic work-up for abdominal pain), the investigators generated models of the femoral head and neck of 4,888 children and adolescents. Notably, after the age of 9 years, the epiphyseal tubercle height was smaller in subjects with obesity than in those of normal weight. Furthermore, cupping height at the superior peripheral aspect of the epiphysis, adjacent to the site of the epiphyseal tubercle, was larger in subjects with obesity before the age of 11 years. However, at a time when the cupping height normally increases—after age 13—it became smaller in the subjects with obesity than in those of normal weight. Subjects with obesity also had more retroversion of the epiphysis throughout childhood until 15 years of age. This study presents good evidence that, in children with obesity, the osseous topography of the proximal femoral physis is abnormal, predisposing it to disengagement of physeal interdigitations, i.e., to SCFE. The cause of this is unclear. Perhaps inhibition of normal physeal development in children with obesity is another example of the Hueter-Volkmann principle at work. A weakness of the study is that the measurement differences between the 2 groups, in absolute terms, were modest. However, given the impressively large size of the cohort, the findings are highly likely to be accurate, and reproducible. How do we know that the differences are clinically important? As the authors note, the cumulative effect of small changes to the structure of the physis may put it at risk for failure. Finite element analysis might be one way to confirm this. Which children with obesity are at greatest risk for developing SCFE? Certain hormones are known to have detrimental effects on the cellular physiology of the growth plate. Hyperinsulinism and high circulating levels of leptin have each been strongly associated with SCFE4,5. Does hormonal disruption of normal cellular physiology of the growth plate contribute to the abnormal bone development illustrated by the present study? Basic science research might address these questions. From a clinical perspective, the methods used and the findings of the present study could lead to a more precise predictive model for the determination of which children are at greatest risk for SCFE. Perhaps similar technology to that used by Novais et al. might be used to analyze radiographs of the hips to detect early indications of SCFE.